Human RCC Binding Protein in Prostate Cancer Cell Line DU145
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Epithelial Cell, Cell Culture
DISEASE(S): Prostate Adenocarcinoma
SUBMITTER: 
Lizhong Wang
LAB HEAD: Lizhong Wang
PROVIDER: PXD056404 | Pride | 2025-07-23
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| RCC2.csv | Csv | |||
| RCC2.mgf | Mgf | |||
| RCC2.mzML | Mzml | |||
| checksum.txt | Txt | |||
| control.csv | Csv |
Items per page: 5 1 - 5 of 7 |
Similar Datasets
Project description:Type II germ cell tumors (GCTs) are with more than 90% the most common neoplasia in young men of age 14 - 45 years. It is generally accepted that GCTs arise from a common precursor lesion, called germ cell neoplasia in situ (GCNIS), eventually developing into seminomas or non-seminomas. The non-seminomatous stem-cell like embryonal carcinomas (EC) can further differentiate into teratomas (TE), yolk sac tumors (YST), or choriocarcinomas (CC). Orchiectomy followed by chemo- or radiotherapy is a widely used procedure in the treatment of type II GCTs, leading to high cure rates of up to 90%. Nevertheless, about 10 - 15% of patients with progressive disease relapse as a result of drug resistance and are condemned for a poor prognosis and a short survival of only a few months. Cluster of differentiation 24 (CD24) is a small, mucin-like glycosylphosphatidylinositol (GPI) anchored membrane molecule that functions both, in signal transduction and as an adhesion molecule. This glycoprotein is mainly expressed on the surface of hematopoietic, neural, muscular, and epithelial cells. Moreover, CD24 has been implicated in tumor metastasis, as fucosylated CD24 interacts with P- and E-selectin, allowing invasion of tumor cells to distal sites. High expression or amplifications of CD24 has been described in a variety of solid malignancies, such as non-small cell lung carcinoma, gliomas, breast cancer, retinoblastoma, hepatocellular carcinoma, renal cell carcinoma, cervical carcinoma, prostate cancer, urothelial carcinoma, pineal parenchymal tumors, and ovarian cancer. In this study, we investigated the putative function of CD24 and its interaction partners in (cisplatin-resistant) GCT cell lines by generating CD24-deficient EC cells by CRISPR/Cas9-mediated gene editing. Changes in the proteome between CD24-deficient cells and parental cells were measured by liquid-chromatography coupled with mass spectrometry (LS-MS).
2022-01-19 | PXD025110 | Pride
Project description:The CD24 cell surface receptor promotes apoptosis in developing B cells, and we recently found that it induces B cells to release plasma membrane-derived, CD24-bearing microvesicles (MVs). Here we have performed a systematic characterization of B cell MVs released from WEHI-231 B lymphoma cells in response to CD24 stimulation. We found that B cells constitutively release MVs of approximately 120 nm, and that CD24 induces an increase in phosphatidylserine-positive MV release. RNA cargo was predominantly comprised of 5S rRNA, regardless of stimulation; however, CD24 caused a decrease in the incorporation of protein coding transcripts. The MV proteome was enriched with mitochondrial and metabolism-related proteins after CD24 stimulation; however, these changes were variable and could not be fully validated by western blotting. CD24-bearing MVs carried Siglec-2, CD63, IgM, and, unexpectedly, Ter-119, but not Siglec-G or MHC-II despite their presence on the cell surface. CD24 stimulation also induced changes in CD63 and IgM expression on MVs not mirrored by the changes in cell surface expression. Overall, the composition of these MVs suggests that they may be involved in releasing mitochondrial components in response to pro-apoptotic stress with changes to the surface receptors potentially altering the cell type(s) that interact with the MVs.
2017-09-01 | PXD005919 | Pride
Project description:CD24 plays a crucial role in tumor growth and metastasis, including in prostate cancer. While CD24 stimulates prostate cancer cell growth by controlling the ARF-NPM interaction and p53 inactivation, the mechanism of CD24-mediated metastasis remains elusive. This study identifies a direct interaction between CD24 and RCC2 with roles in prostate cancer cell proliferation and migration. Immunohistochemical analysis of primary prostate cancer samples showed expression of CD24 in 49% of samples and RCC2 in 82%, with a positive correlation between their protein levels. Their co-expression, particularly the binding of CD24 to the C-terminal domain of RCC2, supports their direct interaction, which may regulate cell motility and adhesion. Functional assays revealed that knockout (KO) of RCC2 in DU145 and PC3 prostate cancer cells inhibited cell proliferation but unexpectedly enhanced cell migration and invasion, while CD24 KO reduced proliferation and migration. Notably, dual KOs of CD24 and RCC2 led to a significant decrease in cell proliferation but showed mixed effects on migration, indicating a complex interplay between these proteins. In vivo, RCC2 KO in prostate cancer cells promoted spontaneous lung metastasis without significantly altering primary tumor growth, contrasting with CD24 KO, which reduced tumor growth and metastasis. Mechanistically, RCC2 was shown to ubiquitinate and degrade Vimentin, influencing cytoskeletal dynamics and migratory behavior. Furthermore, CD24 was found to ubiquitinate and degrade RCC2, leading to modulation of the β-catenin signaling pathway. RCC2 KO increased β-catenin activation and decreased the expression of its inhibitors AXIN2 and APC, while CD24 KO led to β-catenin inactivation. This opposing regulation of β-catenin signaling by CD24 and RCC2 underscores their differential roles in prostate cancer cell migration. These findings provide new insights into the molecular mechanisms underlying prostate cancer growth and metastasis and identify the CD24-RCC2 axis as a potential therapeutic target for controlling tumor growth and metastasis in prostate cancer.
2025-07-21 | GSE277962 | GEO
Project description:We endeavored to identify factors and pathways regulated by CD24 and to obtain leads regarding the mechanism by which CD24 inhibited the invasiveness and metastasis of pancreatic cancer cells by performing cDNA microarray analysis on S2-013 CD24 RNAi clones and control clones. The group of genes showing increased expression was mainly comprised of genes for molecules with functions related to RNA metabolism, transcription factors, proteases, and molecules involved in embryonic development and cell growth. The set of genes downregulated by knockdown of CD24 included the target mRNAs of a phosphorylation-dependent endoribonuclease G3BP that interacted with CD24. The target mRNAs of G3BP were identified in GSE17056. These results suggested that CD24 inhibited the RNase activity of G3BP, and that a function of CD24 was to inhibit the degradation of specific mRNAs. Transcripts upregulated or downregulated by knockdown of CD24 were identified through expression profiling of a total of 12,135 genes in S2-013 CD24 RNAi clones compared to control clones. Before labeling with Cy5 or Cy3, total RNA from two S2-013 CD24 RNAi clones were mixed and total RNA from two control clones were mixed. The supplementary files 'GSE17055_higher_siCD24.txt' and 'GSE17055_higher_control.txt' list the differentially expressed genes.
2010-06-24 | E-GEOD-17055 | biostudies-arrayexpress
Project description:Purpose: The aim of the present study was to identify and characterize in tissue samples of clear cell-renal cell carcinoma (ccRCC) a population of CD133+/CD24+ cancer cells (RCC-derived cells-RDCs) and to study the differences with their nonneoplastic counterpart, tubular Adult Renal Progenitor Cells (ARPCs). Materials and methods: CD133+/CD24+ RDCs were isolated from 40 patients. The mesenchymal phenotype and stemness proteomic profile of these RDCs were characterized. The colony-forming efficiency and self-renewal ability were tested with limiting dilution. The tumorigenic properties were evaluated in vitro with Soft Agar Assay. The angiogenic response was evaluated in vivo with the chorioallantoic membrane angiogenic assay. Microarray analysis was performed on 6 tARPCs and 6 RDCs clones. Expression of membrane proteins was evaluated with flowcytometry and immunofluorescence staining. Results: CD133+/CD24+ cells were isolated from normal and tumoral kidney tissue. FACS analysis showed that RDCs did not express the mesenchymal stem cell markers. We showed that CD133+/CD24+ tumor cells were more undifferentiated than tARPCs. RDCs were clonigenic and able to differentiate into adipocytes, epithelial and osteogenic cells. RDCs were able to regenerate tumor cells in vitro and to induce angiogenesis in vivo. The gene expression profile identified CTR2 as a membrane marker for this neoplastic population. Conclusions: Our results indicate the presence, in ccRCC, of a CD133+/CD24+/CTR2+ cancer cells population. These cells possess some stem cell-like features, including in vitro self-maintenance and differentiating capabilities, and are able to induce an angiogenic response in vivo.
2015-12-15 | GSE48550 | GEO
Project description:How disseminated tumor cells (DTCs) engage specific stromal components in distant organs for survival and outgrowth is a critical but poorly understood step of the metastatic cascade. Previous studies have demonstrated the importance of the epithelial-mesenchymal transition (EMT) in promoting the cancer stem cell properties needed for metastasis initiation, while the reverse process of mesenchymal-epithelial transition (MET) is required for metastatic outgrowth. Here we report that this paradoxical requirement for simultaneous induction of both MET and cancer stem cell traits in DTCs is provided by bone vascular niche E-selectin. Using cell surface alkoxyamine-biotinylation and label-free LC-MS/MS, Glg1 was identified as a top candidate Fut3/Fut6-dependent E-selectin ligand. We functionally validated their involvement in the formation of bone metastasis. These findings provide unique insights into the functional role of E-selectin as a component of the vascular niche criticalfor metastatic colonization in bone.
2019-11-13 | PXD012942 | Pride
Project description:We endeavored to identify factors and pathways regulated by CD24 and to obtain leads regarding the mechanism by which CD24 inhibited the invasiveness and metastasis of pancreatic cancer cells by performing cDNA microarray analysis on S2-013 CD24 RNAi clones and control clones. The group of genes showing increased expression was mainly comprised of genes for molecules with functions related to RNA metabolism, transcription factors, proteases, and molecules involved in embryonic development and cell growth. The set of genes downregulated by knockdown of CD24 included the target mRNAs of a phosphorylation-dependent endoribonuclease G3BP that interacted with CD24. The target mRNAs of G3BP were identified in GSE17056. These results suggested that CD24 inhibited the RNase activity of G3BP, and that a function of CD24 was to inhibit the degradation of specific mRNAs.
2009-07-23 | GSE17055 | GEO
Project description:The study was a comparison of gene expression using RNA-seq. We analyzed the stem and progenitor cells from WT and Vav-cre+ Tet2fl/fl Flt3-ITD (T2F3) mice. We isolated stem cells LSK (lin- sca+ kit+) and granulocyte-macrophage progenitors GMP (lin- sca- kit+ fcgr+ cd34+) cells from bone marrow. Comparisons were made across genotypes WT vs. T2F3 and cell types LSK vs. GMP. Comparison of WT and Tet2-/-Flt3ITD bone marrow stem and progenitor cells.
2015-05-01 | E-GEOD-57244 | biostudies-arrayexpress
Project description:Purpose: The aim of the present study was to identify and characterize in tissue samples of clear cell-renal cell carcinoma (ccRCC) a population of CD133+/CD24+ cancer cells (RCC-derived cells-RDCs) and to study the differences with their nonneoplastic counterpart, tubular Adult Renal Progenitor Cells (ARPCs). Materials and methods: CD133+/CD24+ RDCs were isolated from 40 patients. The mesenchymal phenotype and stemness proteomic profile of these RDCs were characterized. The colony-forming efficiency and self-renewal ability were tested with limiting dilution. The tumorigenic properties were evaluated in vitro with Soft Agar Assay. The angiogenic response was evaluated in vivo with the chorioallantoic membrane angiogenic assay. Microarray analysis was performed on 6 tARPCs and 6 RDCs clones. Expression of membrane proteins was evaluated with flowcytometry and immunofluorescence staining. Results: CD133+/CD24+ cells were isolated from normal and tumoral kidney tissue. FACS analysis showed that RDCs did not express the mesenchymal stem cell markers. We showed that CD133+/CD24+ tumor cells were more undifferentiated than tARPCs. RDCs were clonigenic and able to differentiate into adipocytes, epithelial and osteogenic cells. RDCs were able to regenerate tumor cells in vitro and to induce angiogenesis in vivo. The gene expression profile identified CTR2 as a membrane marker for this neoplastic population. Conclusions: Our results indicate the presence, in ccRCC, of a CD133+/CD24+/CTR2+ cancer cells population. These cells possess some stem cell-like features, including in vitro self-maintenance and differentiating capabilities, and are able to induce an angiogenic response in vivo. Study of gene expression profiling of Renal Cancer Cells (RCSCs), tubular Adult Renal Progenitor Cells (tARPCs), Renal Proximal Tubular Cells (RPTEC) and Mesenchymal Stem Cells (MSC). To highlight the similarities and the differences with known renal stem populations and with terminally differentiated renal cells, for each patient, 6 subcultures of tubular ARPCs (tARPCs), 3 subcultures of the MSC and 3 subcultures of the RPTEC were included in the analysis.
2015-12-15 | E-GEOD-48550 | biostudies-arrayexpress
Project description:The RAG1 endonuclease, together with its cofactor RAG2, is essential for V(D)J recombination but is a potent threat to genome stability. The sources of RAG1 mistargeting and the mechanisms that have evolved to suppress it are poorly understood. Here, we report the surprising finding that RAG1 binds to thousands of sites in the genome of developing lymphocytes, primarily at active promoters and enhancers. The genome has responded by reducing the abundance of "cryptic" recombination signals near sites of RAG1 binding. This depletion operates specifically on the RSS heptamer, with nonamers enriched at RAG1 binding sites. Reversing this RAG-driven depletion of cleavage sites by insertion of strong recombination signals creates an ectopic hub of RAG-mediated V(D)J recombination and chromosomal translocations. Our findings delineate rules governing RAG binding in the genome, identify areas at risk of RAG-mediated damage, and highlight the evolutionary struggle to accommodate programmed DNA damage in developing lymphocytes. MNase-seq profiles of mouse thymocytes
2015-08-06 | E-GEOD-69474 | biostudies-arrayexpress